Frontiers in aging neuroscience · 2026
Short-term environmental enrichment modulates brain region-specific redox responses in adolescent female mice.
СтатьяНазвание и аннотация: Перевод в очереди
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de Sousa Fernandes Matheus Santos, Kanashiro Alexandre, Ramos Tiago Lacerda, Pereira Danielle Dutra, de Souza Vanessa Lima, Lagranha Claudia Jaques, Tüfekci Sacide, Yagin Burak, Alkhamees Nouf H, Souto Fabrício Oliveira
Аннотация
BACKGROUND: Environmental enrichment (EE) is a non-pharmacological intervention known to enhance neuroplasticity and resilience. However, studies of EE on brain redox balance have focused predominantly on males and single regions, leaving the developing female brain and region-specific responses largely uncharacterized. This study investigated the effects of a three-week EE protocol on oxidative balance in the hippocampus, hypothalamus, and brainstem of adolescent female C57BL/6 mice.
METHODS: Lipid peroxidation was measured by thiobarbituric acid reactive substances (TBARS), and protein oxidation by carbonyl content. The enzymatic antioxidant system was evaluated through the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST). Non-enzymatic antioxidant defenses included quantification of reduced glutathione (GSH), oxidized glutathione (GSSG), the GSH/GSSG ratio, and total sulfhydryl content, providing an integrated assessment of redox homeostasis.
RESULTS: In the hippocampus, EE promoted a dual redox profile characterized by increased TBARS alongside reduced protein carbonylation, increased SOD activity, decreased GSSG, and elevated total sulfhydryl content. In the hypothalamus, EE exerted a protective effect, reducing both lipid and protein oxidation without altering enzymatic antioxidant activities. Instead, non-enzymatic defenses were selectively enhanced, as evidenced by increased GSH and sulfhydryl levels. In the brainstem, EE reduced oxidative damage markers and selectively increased SOD activity, while other antioxidant systems remained unchanged.
CONCLUSION: Collectively, all regions exhibited reduced protein oxidative damage in our female-inclusive study design, but through different patterns: a dissociated hippocampal profile (increased TBARS with reduced protein oxidation and higher SOD/sulfhydryls), non-enzymatic thiol-based buffering in the hypothalamus, and SOD-centered defense in the brainstem, supporting a context-dependent model of oxidative regulation.
METHODS: Lipid peroxidation was measured by thiobarbituric acid reactive substances (TBARS), and protein oxidation by carbonyl content. The enzymatic antioxidant system was evaluated through the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST). Non-enzymatic antioxidant defenses included quantification of reduced glutathione (GSH), oxidized glutathione (GSSG), the GSH/GSSG ratio, and total sulfhydryl content, providing an integrated assessment of redox homeostasis.
RESULTS: In the hippocampus, EE promoted a dual redox profile characterized by increased TBARS alongside reduced protein carbonylation, increased SOD activity, decreased GSSG, and elevated total sulfhydryl content. In the hypothalamus, EE exerted a protective effect, reducing both lipid and protein oxidation without altering enzymatic antioxidant activities. Instead, non-enzymatic defenses were selectively enhanced, as evidenced by increased GSH and sulfhydryl levels. In the brainstem, EE reduced oxidative damage markers and selectively increased SOD activity, while other antioxidant systems remained unchanged.
CONCLUSION: Collectively, all regions exhibited reduced protein oxidative damage in our female-inclusive study design, but through different patterns: a dissociated hippocampal profile (increased TBARS with reduced protein oxidation and higher SOD/sulfhydryls), non-enzymatic thiol-based buffering in the hypothalamus, and SOD-centered defense in the brainstem, supporting a context-dependent model of oxidative regulation.